Neuro Flashcards
What is the difference between focal and generalised seizures?
- Focal - specific neuro deficit within one region (e.g. temporal) with retained/impaired consciousness.
- Generalised - simultaneous involvement of both hemispheres with LoC.
What is Jacksonian March?
A type of focal seizure of abnormal electrical activity in the frontal lobe where clonic movements (contracting and then relaxing) start in one limb and move proximally through the body.
Seizures can be classified by 3 modes - what are they?
- Seizure typeLocation (focal/generalised) & motor/non-motor onset
- Level of awareness aware/impaired awareness
- Other features
List the 5 main epilepsy childhood syndromes according to onset:
* 6mo
* 6-10mo
* 1-5yrs
* 6-8yrs
* Teenage
- West syndrome (full body spasms, poor prognosis, 4-8mo)
- Dravet’s syndrome (prolonged febrile convulsions)
- Lennox-Gastaut syndrome (similar to West syndrome but presents later)
- Benign rolandic epilepsy (focal, facial/tongue/speech paraesthesia often in morning, most common)
- Juvenile myoclonic epilepsy (full myoclonic seizures often following sleep deprivation)
What are the EEG changes expected in West’s, Lennox Gastaut’s and Benign Rolandic Epilepsy?
West’s - hypsarrhythmia
L-G - slow spikes
BRE - centrotemporal spikes
Epilepsy
State the investigations you would do/consider
- Bloods - glucose, U&E
- EEG
- ECG
- MRI Brain
- Other - LP, urine cultures, ?septic screen
Management for seizures
- community
- hospital
Define status epilepticus
-
Community: Rectal Diazepam or Buccal Midazolam
* Hospital: IV Lorazepm (–> repeat after 10 mins if continue) –> IV Phenobarbitone –> I+V. - Prolonged seizure for >5 minutes or 2 seizures without regaining consciousness in between.
3 crtiteria for a brain MRI for investigatiing seizures
- If seizure happened before age of 2
- If unresponsive to 1st line anti-epilpetics
- Focal seizures
Usually anti-epileptics are started after the second seizure. NAme the 4 criteria for reasons to start after 1st sezirue.
- Type of seizure:Focal
- EEG findings: unequivocal activity
- Further seizure is perceived an unacceptable risk
- MRI findings: structural abnormality
note after first seizure cannot drive for 6 months (need to inform DVLA)
Anti-epileptic 1st and 2nd lines for
- generalised motor
- focal
- Absence
- myoclonic (type of generalised absence)
For male (*Sodium Valproate CI for women at reproductive age)
- (1) Sodium valproate (2) Lamotrigine/Levetiracetam
- (1) Lamotrigine/Levetiracetam (2) Carbamazepine
- (1) Ethosuximide (2) Sodium Valproate/Lamotrigine
- (1) Sodum valproate (2) Levetiracetam
Generalised –> generalised absence –> generalised absence myoclonic = C –> E –> L. As the seizure type gets more specific the second line drug is later in the alphabet.
Treatement for West Syndrome
Prednisolone (reduces spasms) / Vigabatrin (inhibits breakdown of GABA)
MOA of
- Sodium Valproate (pleiotropic)
- Carbamazepine/Lamotrigine/Phenytoin
- Increased activity of GABA and Na+/Ca2+ channel blockers (stabilsing membrane potential)
- Na2+/Ca2+ channel blockers
Sodium valproate is the boss drug of epilepsy so makes sense to have multiple mechanisms …..and to be for men (not to be sexist)
Which drug is teratogenic & SEs include liver damage, hair loss & tremor
Sodium Valproate (avoid in woman of reproductive age)
Which drug is a P450 inducer & can cause SEs of agranulocytosis and aplastic anaemia
defiency in granulocytes (basophils, neutrophils and eosinophils) -severe form of neutropenia
Carbamazepine
Phenytoin’s SEs are folate and vitamin D deficiency - what can this lead to?
Megaloblastic anaemia and osteomalacia respectively
3 side effects of Lamotrigine
Stevens Johnson syndrome (rash –> shedding of skin), DRESS syndrome, leucopenia
drug reaction wth eosinophilia and systemic symptoms - rash but with organ invovement (lymphadenopathy, fever)
Define status epileptics and its immediate treatment.
What are the 2nd, 3rd and 4th line options if this fails?
Seizure lasting >5 mins or 2+ seizures in 1hr.
1) A-E; IM Lorazepam
2) IV Lorazepam (repeat after 10 mins)
3) IV Phenytoin
4) Thiopentate sodium (anaesthesia)
How do you treat status epilepticus in the community? (Buccal or rectal)
Buccal Midazolam
Rectal Diazepam
Clinical features of a cluster headache
Prophylaxis - 1st line
Treatment
- Severe onset, localised, severe pain
- repeated episodes (clusters of attacks) –> disappear –> reappear
- acute episodes approx 0.5-2hrs long, often same time each day over a few weeks
- red, swollen, watery, miotic eye
- sweating, nasal discharge
Prophylaxis
- Verapamil
Treatment
- Sumatriptans SC
Oxygen
Differential: SAH, migraine, venous sinus thrombosis, GCA
4 types of migraine
With aura
Without aura
Hemiplegic migraine (stroke mimic)
Silent migraine (aura, no headache)
Prophylactic medical treatments for cluster headaches (3) vs migraine (3)?
Cluster - Verapamil (CCB), Lithium, Prednisolone
Migraine - Propanolol, Topiramate (teratogenic), Amitryptiline
Medical treatment options for cluster vs migraine (acute & prophylactic options)
Cluster - Triptans (S/C); O2
Migraine - Triptan+ NSAID/paracetamol.
Migraine prophylaxis - Topiramate or Propanolol.
Class of triptans
5HT receptor agonsits; MOA not fully known but may reduce peripheral pain signals
Clinical features of meningitis vs meningococcal septicaemia
Most common cause of viral meningitis
Meningitis = headache, neck stiffness (in some), photophobia, fever, vomiting, seizure (bacteria/virus in CSF around brain and spinal cord)
Meninogococcal septicaemia (meningococcus in bloodstream) = presence of non-blanching haemorrhagic rash
Viral meningitis - enteroviruses like coxsackie
Investigations for meningitis in hospital (3 main ones)
- Lumbar puncture- CSF analysis (culture, neutrophils, glucose, protein, PCR)
- Blood glucose (to compare against CSF glucose)
- Bloods - Meningococcal PCR (quicker than culture)
note neutrophils suggestive of bacterial meningitis rather than other causes like HSE.
Community vs hospital management for meningitis?
Community - suspected meningitis + non blanching rash–> start Benzylpenicillin and immediate transfer to hospital.
Hospital
- abx as per trust guidelines and dependent on age
+/- steroids dependent on LP results
- fluids and cerebral monitoring
Abx treatment for bacterial meningitis; how does it vary for children <3 months?
<3 months: Cefutaxime + Amoxicillin (to cover for listeria contracted during pregnancy)
>3 months: Ceftriaxone (because Cefutaxime can cause dangerous increase in bilirubin)
or according to local guidelines
Secondary causes of headache - intracranial (list 5), extracranial (list 5)
Intra = meningitis, haemorrhage (SAH/ICH) venous sinus thrombosis, temporal arteritis/GCA, raised ICP
Extra = acute angle closure glaucoma, pre-eclampsia, encephalitis, carotid artery dissection, sinusitis
Raised ICP: presentation & examination findings
Presentation: worse in morning with coughing & bending. Nausea & vomiting. Reduced GCS. Visual disturbance/neurological syx/seizures.
Examination: Reduced GCS. Pupil dilation. Papilloedema. CN III palsy (late). Cushing’s (if herniated). Cheyne Stokes respiration.
Herpes simplex encephalitis is most common cause of sporadic encephalitis.
The virus typically affects which lobes, causing which typical symptoms?
Ix: CT head & LB. Findings?
Mx?
- Temporal lobes
- Headache, fever, seizure
- Focal sx - aphasia
- CT - Hypodensities/ptetchial haemorrhages in temporal lobes (aka bitemporal lobe changes)
- LP - raised WCC & proteins.
- IV Aciclovir
Risk factors for venous sinus thrombosis?
Hypercoaguable state (pregnancy)
Venous sinus thrombosis - presentation, investigations & management
Presentation: headache, N&V, seizures, features of raised ICP, focal neurology.
Investigations: CT venography
Management: LMWH + antibiotics (high risk of infection)
GCA presentation, investigations(3) and managementy - how does this vary for if there is visual involvement?
Presentation: over 55, temporal headache, scalp tenderness & jaw claudication, ipsilateral blindness, papilloedema.
Investigations:
1. Bloods - raised ESR,
2. Duplex temporal artery - (assess speed and volume of blood) - “halo” sign, stenosis
3. Biopsy temporal artery - multinucleated cells/skiplesions
Management: high dose glucocorticoids
Evolving visual defect: Methylpred then Pred
No visual defect: Pred
Primary causes of headache
Tension headache
Cluster
Migraine
Typical presentation of neurogenic thoracic outlet syndrome?
Pressure on bracchial plexus –> wasting of thenar eminence, hand weakness (worsened by raising above head), +/- paraesthesia +/- autonomic symptoms
Typical presentation of vascular TOS?
vascular: pressure on subclavian artery or subclavian vein.
Artery - claudication.
Vein - arm swelling.
Features of Tremor
* Parkinsonism
* Benign Essential Tremor
* Cerebellar disease
* Anxiety
* Thyrotoxicosis
* Hepatic encephalopathy
* CO2 retention
* Renal failure (uraemia)
- Asymmetrical, resting tremor (“pill rolling”), relieved by voluntary movement. Associated with bradykinesia / problems with dexterity/fine movement
- Symmetrical, alleviated by alcohol and rest, worse if arms outstretched.
- Intention tremor, impaired finger-nose test.
- Symmetrical, worse under stress. Hx of MH.
- Associated with thyrotoxic signs
- Asterixis (flapping tremor) - bilateral, postural. Hx of CLD.
- Asterixis (flapping treor) - bilateral, postural. Hx of COPD.
- Same
Motor Neurone Disease
* brief definition
* subtypes, relative prognosis and whether UMN/LMN signs are affected (4)
* risk factors (3)
* sx presentation and important negatives (3)
* only licensed treatment available:
- MND is a neurodegenerative condition twhich ultimately results in paralysis.
- ALS (50% of cases, both UMN/LMN sx, 2-5 yr prog)
- PMA (7-8yrs, LMN)
- PLS (10 yrs, UMN)
- PBP (<1 yr, both)
- Genetics (10%), idiopathic, physical activity, male, increasing age
- Progressive muscle weakness or bulbar symptoms. Negatives - spares ocular & pelvic floor muscles - x oculomotor disturbance, x incontinence - until late stage.
- Riluzole (glutamate antagonist)
Distinguish bulbar palsy from pseudobulbar palsy
Both affect the cranial nerves 9,10,11,12 found on the medulla of brainstem - involved in function of muscles of face, mouth and tongue. Both cause tongue muscle wasting +
* Bulbar palsy- LMN signs - fasciculations
* Pseudobulbar palsy - UMN - exaggerated jaw jerk relfex, tongue spasticity
Multiple scerlosis
* Definition
* Disease patterns (4)
* Risk factors (3)
* General presentation, and common types (3)
* Diagnosis (2) and investigations (2)
* Management - MDT & Neuro rehab team. Long term treatment class and medx for relapse
* First line treatment options for spasticity (2)
- A chronic progressive condition caused by demyelination and plaque formation of the CNS neurons. Often autoimmune attack against the myelin sheath.
- Clinically isolated episode (technically not MS yet)
- Relapsing-remitting (most common)
- Secondary progressive (R/R then continue progressing)
- Primary progressive (without R/R)
- Female sex, EBV, genetics, smoking, obesity
- present with variable sx depending on which part of CNS is affected (5 - motor, sensory, visual, cerebellar, autonomic)
- Based on CNS lesions “disseminated in time & space & greater than 1 yr in nature.
- MRI Brain & spial cord - plaques.
- LP - oligoclonal bands (antibodies) in CSF.
- DMARDS
- Corticosteroids for relapse (Methylpred)
Multiple-sclerosis: management
To reduce relapse: DMARDS
- types and general mechanism
To treat relapses: croticosteroids
- type
- Symptomatic treatment
- treatments for 5 main symptoms
Conservative
- Exercise, weight loss, smoking cessation
- (physio, OT)
- Fingolimod (S1P modulator) and Natalizumab (anti-A4B1) - biologic therapy- target specific leucoytes/interleukins to reduce immission.
-
Methylprednisolone
*- Limb spasticity - Baclofen/Gabapentin & physiotherapy - Fatigue - Amantine & CBT
- Depression - SSRIs & CBT
- Urge incontinence - anticholinergics
- Neuropathic pain - Amitryptiline/Gabapentin
Visual effects
- Optic neuritis (3 key sx, examination finding?, cause other than MS)
- Internuclear opthalmoplegia
- Conjugate gaze palsy (CN 6)
- Double vision
- Uhthoff’s
Optic neuritis
1. **Visual **- cloudy vision, red desaturation, central scotoma
2. Pain - worse on mvmnt
3. RAPD
4. O/E - papilloedema
Cause - MS, syphillis, autoimmune conditions (SLE, DM), viruses (measles, mumps)
INO
damage to medial longitudinal fasciculus between CN3 (oculomotor) and CN6 (abducens)
- inability to adduct affected eye and horizontal nystagmus of opposite eye
Conjugate gaze palsy
inability to both both eyes together in straight line
Double vision
noted on H test (CN I)
Uhthoff’s
visual changes are worsened by rise in body temp
Internuclear opthalmoplegia
- Demyelination or any damage to the MLF - medial longitudinal fasciculus (connection between CN3 and CN6)
- inability to adduct eye of affected side and nystagmus of other eye
Transverse myelitis
-definition; trigger
- symptoms below the level of the cord?
- L’hermitte’s sign?
- treatment
- Focal inflammation extending across the spinal cord - triggered by infectious or autoimmune process
- Motor and sensory sx below level of cord
- E.g. L’hermitte’s sign = sensory dissturbance (electric shock down back of neck/back - due to demyelination within cervical spinal cord) and tight-band sensation around trunk
- Dexamethasone
Wet, wobbly & wacky
(urinary incontinence, recurrent falls and dementia) is the classical triad for what?
What causes it?
Risk factors?
What therefore would you not expect?
Typical finding on cxr - or not a finding?
Mx?
Normal pressure hydrocephalus
* reversible dementia
* reduced absorption of CSF at the arachnoid villi –>progressive fluid build-up in brain -> develop sx over few months as large ventricles obstruct brain tissue
* increasing age, head injury, stroke, CNS infection
* x papilloedema/raised ICP
* cerebral imaging shows ventriculomegaly with lack of sulcal enlargement (aka ventricles are bigger but not causing raised ICP)
* mx - ventriculoperitoneal shunt
Gait abnormalities - cause, features
* Hemiplegic
* Diplegic
* Parkinsonian
* Ataxic
* Neuropathic
* Myopathic
* Antalgic
Involuntary movements
* Choreiform
* Akathitosis
* Ballismus
-
Circumduction. UMN lesion (e.g. stroke) - spastic weakness of lower limbs.
Scissoring. (overlapping of lower limbs). Bilateral CVA (stroke), spinal cord lesion, MND. - Shuffling –> festinant gait w slow initiation, reduced stride length, reduced arm swing, and stooped posture. PArkinson’s disease/PD+/drugs/viral.
- Broad based staggering. Problem with balance: cerebellum, vestibular system or proprioception. E.g. alcoholic cerebella dysfunction, labrynthitis, sensory ataxia from spinl cord lesion/DM.
- High steppage foot drop/toe dragging. - weakness in distal muscles due to peripheral neurapathy. Common peroneal neuropathy (L4,L5,S1) - e.g. L5 radiculopathy or polyneuropathy/CMT.
- Waddling; weakness of hip abductors (minimus/medius). Pelvis dips on unsupported side. Positive Trendelenberg.
- Abnormal gait due to pain - e.g. #, osteoarthritis, RA.
- Chorea - Involuntary dance-like movements. Huntington’s/Sydenham’s.
- Athetosis - slower form of chorea - continuous, writhing movements (“without position)
- Ballismus - severe form of chorea - with violent flinging of limbs
Intracranial venous thrombosis: includes sagittal sinus, cavernous sinus thrombosis and lateral sinus thrombosis. It can result in a stroke/CVA.
- risk factors
- presentation (signs of raised ICP)
- ix and typical finding if sagittal sinus thrombosis
- mx
- hypercoaguable state, smoking
- headache, N+V, LoC
- MRI venography: “empty delta sign”
- anti-coagulants: LMWH
Intracranial hypertension
- risk factors
- presentation
- ix
- mx - lifestyle and medical
- fenale sex, obesity, COCP use, pregnancy, other drugs
- headache worse on bending forward, signs of raised ICP, papilloedema, enlarged blind spot
- MR venogram: “Empty sella sign”
- Weight loss
- Acetazolamide to reduce production of CSF
- +/- topiramate (also beneficial for weight loss)
- surgical options e.g. ventriculoperitoneal shunt
Parkinson’s plus syndromes
- Multisystem atrophy (3 main features)
- Dementia with lewy bodies (distinction from PD)
- Progressive supranuclear palsy (PSP)
- Corticobasal degeneration
Other causes of parkinsonism:
- Drugs
- Infection - viral
- Wilson’s disease
- Trauma
- Toxins
- basal ganglia (PD), cerebellum (ataxia) and autonomic dysfunction
- cognitive decline prior to motor symptoms and often fluctating congition +/- visual hallucinations
- PSP: impaired vertical gaze, instability/falls, parkinsonism, cognitive decline
*
Parkinson’s medication
1st line:
Levodopa
- medicinial forms - what else is co-prescribed and why?
- side effects
2nd line or 1st line if motor symptoms aren’t main problem
Example:
- Dopamine agonists
- MAO-B inhibitors
Adjuncts:
- Antimuscarinics
- COMT-Inhibitors
Levodopa
- Addition of a decarboxylase to prevent breakdown of dopamine before it reaches the brain
- Co-beneldopa (Levodopa and Benserazide)
- Co-careldopa (levodopa + Carbidopa)
- ses: dyskinesias
Dopamine agonists
- Bromocriptine
- Pergolide
- Carbergoline
MAO-B inhibitors
- Rasagline
- Selegiline
Adjuncts
COMT-Inhibitors
…capones
Antimuscarinics
to help DIP primarily for tremor and rigidity
Procyclidine
Benzotripine etc
Bell’s palsy; cranial nerve 7 palsy
* Risk factors
* Presentation
* Management
Risk factors:
- Pregnancy
- 20-40yrs
- ? herpes simplex infection
Px - Sudden onset of
- Ipsilateral paralysis of face including forehead (LMN)
- Hyperacusis/ear ache (facial nerve supplies stapedius muscle)
- Loss of taste (CN VII- anterior 2/3 of tongue)
Mx:
- Prednisolone PO within 3 days
- Eye care (tape closed at night, artificial tears ifn necessary)
-
Herpes simplex encephalitis
- typically affects which lobes?
- typical causative organism?
- Presentation
- Investigations (LP), viral PCR, CT/MRI Brain, EEG - findings
- Mx
- temporal lobes
- HSV type 1
- meningism, seizures, coma
- LP: raised lymphocytes, normal protein, normal glucose
- CT: ptechiae, MRI brain - hyperintensity of temporal lobes, EEG - lateralised periodic discharges at 2Hz
- IV Aciclovir
Myasthenia gravis
Autoimmune condition of the NMJ, autoantibodies to acetylcholine receptor on post synaptic cleft of NMJ
- Presentation
- Fatiguability in muscles can be eliicited by (3)
- autoantibodies (most likely to least)
- ix name
- Positive test if ….
- additional ix if thymoma suspected (strong link)
- mx (2)
- if initial treatment not effective consider
- differentials
- faceFacial/oculomotor problems - ptosis, diplopia, dysarthia, dysphagia;
- limbsProximal limb weakness; fatiguability
- prolonged blinking –> ptosis; prolonged upward gazing –> diplopia, repeated arm abduction –> unilateral weakness
autoantibodies - anti: ACH-R (85%) antiMUSK (muscle specific tyrosine kinase antibodies)
Ix - single fibre electromyography: high sensitivity (>92%)
- CT/MRI thorax - thymus
- Edrophonium test / or neostigmine: IV dose of antiacetylcholinesterase enzymes (blocks breakdown of Ach)
- positive if symptoms improve (temporary rise in ACh at NMJ relieves weakness)
Mx - reversible acetylcholinesterase inhibitors - Pyridostrigmine/Neostigmine & immunosuppression eventually - reduce production of autoantibodies (Prednisolone, Azathioprine etc)
- ?mABs - Rituximab
- thymectomy
- Lambert-Eaten syndrome (NSCLC; squamous), cranial nerve III palsy, Guillan Barre syndrome/Miller Fisher syndrome starts in eyes, myopathy, muscular dystrophy (in MG the CK level is normal unlike in the latter)
What triggers a myasthenic crisis?
What are patients at risk of?
Treatment (2)
- Infection, stress, trauma, menstruatiom
- Respiratory failure due to weakness of resp muscles
- Iv IGs or plasma exchange (plasmapharesis)
- +/- NIV if severe
Muscular dystrophies - genetic conditions causing gradual muscle weakness/wasting
- Paeds: Duchenne’s/Becker’s
- Adults: Myotonic dystrophy
- Other rare forms …..
Duchenne’s/Becker’s
- genetic inheritenace of both
- mutation on gene Xp21 which codes for?
- which is the more severe form?
- Ix - raised CK; definitive diangosis by?
- Mx -??
- Associated with which condition
Duchenne’s
- Presentation and age of onset
- positive sign on examination
- signs other than myopathy
Becker’s
- key distinguishing points (2)
- X-linked recessive
- Dystrophin - endodess for msucle protein
- Duchenne’s: frameshift mutation; becker’s - non frameshift
- Duchenne’s at 5, becker’s at 10
- Genetic testing; definitive
- Steroids to slow progression and creatine supplements
- poor prog, most cannot walk by age 12
- dialted cardiomyopathy
Duchenne’s
- Gower’s sign positive = use arms to stand from squat
- Calf psuedohypertrophy
- progressive proximal muscle weakness from age 5
- intellectual impairment may be present
Becker’s
- develops after 10 years
- rarely have intellectual impairment
Myotonic dystrophy
type of inhertied muscular dystrophy more common in adults (2 types)
- characterising features
- on examination
- associated with which ocular condition (req opthalmoscope)
- myotonia and slurred speech (myotonia of pharyngeal/oral muscles)
- on clenching fist and opening it, slow muscle relaxation
- normal sensation, normal reflexes
- symmetrical weakness proximal>distal
- cataracts
Polymyositis: DOE
- requires ruling out other causes of myopathy (endocirne, electrolyte, toxic etc)
It is an inflammatory myositis due to underlying causes - autoimmune, infection, drugs (statin), CTs
- what cancers is dermatomyositis associated with?
- Bloods - what is raised?
- Diagnosis obtained from..?
- Mx
- ovary,GI,breast
- CK raised
- muscle biopsy
- steroids
**Subacute combined degeneration of the cord **
- Causes
- Presentation (3)
- SAD therefore
- Like MS it can also cause which sign on neck flexion?
- Typical example patient
- Vitamin B12 (pernicious anaemia) or Vitamin E deficiency - degeneration of the spinal cord due to demyelination
- spastic paresis, bilateral- UMN signs below level of cord (x corticospinal) - (but note can have absent ankle reflexes - doesn;t fit with rest)
- loss of vibration/proprioception, bilateal ( xdorsal columns)
- Ataxia, bilateral Romberg’s +ve
- SAD - still in pain (spinothalamic intact)
- L’hermitte’s sign
Post-Chron’s op, presenting with paraesthesia in toes and fingers, clumsiness and ataxia
Friedrich’s ataxia
most common inherited form of ataxia, presents similarly to SADCD
- General presentation
- Affects what other system due to mitochondria dysfunction?
-Spastic paresis, ataxia, and loss of vibration/proprioception
- also note INTENTION TREMOR
- NS, heart and pancreas
Central cord syndrome
- cause
- presentation
- hyperextension of neck, e.g. car injury
- most common form of incomplete cord lesion
- Bilateral spastic paresis UL>LL
- +/- sensory involvement
Complete spinal cord lesions have no function below site of injury. Incomplete have some function (motor/sensory) below site.
Types of incomplete spinal cord lesion (4)
- Brown-Sequard (unilateral signs)
- Central/cervical cord syndrome
- Anterior cord syndrome
- ## Posterior cord syndrome
Anterior cord syndrome
- caused by
- sx
- presentation (motor and sensory deficit)
- Anterior spinal artery occlusion (aortic dissection, sudden disc rupture, tumour compression etc)
- chest/back pain and spinal shock
- Bilateral spastic paresis and bilateral loss of pain/temp sensation
Syringomyelia
- CSF filled cyst in the spinal cord. Starts medially in cord and then expands outwards.
- Treat cause of syrinx or shunt.
- Risk factors
- Presentation
- Chairi malformation (cerebellar herniation); tumours, trauma, meningitis
- Cape-like distribution of loss of pain/temp sensation (superheroes feel no pain) damage to spinothalamic tract
- ## Spastic weakness LL>UL
Neurosyphillis: what is tabes dorsalis
- wasting of the dorsal columns
- loss of proprioception/vibration sensation
Degnerative cervical myelopathy
Risk factors
Presentation
What is Hoffmann’s sign?
Investigation and finding
Mx - requires urgent insput from..
Definitive surgery
Differentials (2)
- Smoking, genetics, occupation (high axial loading)
- Neck or limb pain
- Loss of motor function +/- sensory/autonomic sx
- Impaired gait and balance
E.g. neck pain, loss of digital dexterity and clumsiness
- MRI Spine- disc degeneration and ligament hypertrophy
- Urgent neurosurgical assessment
- Decompressive surgery
Differentials
- Carpal tunnel syndrome
- Cervical disc prolapse
Cerebellar syndrome
- Symptoms (DANISH)
- Causes
Symptoms
Dysdiadokinesia
Ataxia
Nystagamus (horizontal)
Intention tremor, impaired finger-nose test
Slurred staccato speech
Hypotonia, impaired heel-shin test
Causes
- Friedrich’s ataxia (most common hereditary cause: ataxia, spastic weakness, impaired dorsal columns + intention tremor. Affects heart & pancreas too)
- SACDC (ataxia, bilateral spastic weakness [UMN], impaired proprioception/vibration sense)
- Alcoholic liver disease
- Multiple sclerosis
- Pareneoplastic (lung cancer)
- Drugs: phenytoin, lead poisoning
- Cerebellar stroke
- Cancer - cerebellar haemangioma
- Ataxic telangectasia
- Multisystematrophy (parkinson’s plus syndrome)
Brain abscess
May be caused by sepsis from middle ear/sinuses, trauma/surgery to scalp, penetrating head injury or embolism (endocarditis).
Presenting sx depend on site of abscess -other general signs:
Ix -
Mx - surgical and abx following
Px - fever, raised ICP signs (papilloedema, nausea, seizures), focal neurology, headache (dull, persistent)
Ix - non-contrast CT head
Mx - craniotomy + debridement
IV Abx - Cephalopsorin + Metronidazole
Manage raised ICP - Dexamethasone
Facial nerve palsy
Supply - face, ear, taste, tear
Face - muscles of facial expression (motor)
Ear - nerve to stapedius (causing hyperacusis, ear pain)
Taste - supplies anterior 2/3 of tongue
Tear - paraysympathetic fibres to lacrimal glands
Causes of bilateral facial nerve palsy? (4 main)
Causes of unilateral?
Bilateral
- Sarcoidosis
- GBS
- Lyme disease
- Bilateral acoustic neuroma (Neurofibromatosis type 2)
- Bell’s (unlikely)
Unilateral
LMN - all include forehead
- Bell’s
- Ramsay hunt (VZV)
- Parotid tumour
- MS
- HIV
- DM
UMN
- stroke (forehead sparing)
TIA: sudden onset focal neurology caused by brain, spinal cord or retinal ischemia, without acute infarction (generally features resolve in 1hr
Managenent;
1. Immediate antithrombotic
2. Specialist review with stroke team - urgent (criteria x3?)within 24hrs or within 7 days
Ix - recommend CT ehad not done unless clinical suspcion of alternative diagnosis. What is the preferred method ofimaging if required - same day or at specialist assessment?
Further management? Like stroke
- Aspirin 300mg (unless bleeding disorder, on anticoagulant/low-dose aspirin anyway, contraindications)
- Urgent if suspected cardioembolic source/severe carotid stenosis/crescendo TIA.
Review within 24hrs if suspected TIAin last 7 days, otherwise if longer can be seen wtihin 7 days
Imaging: MRI diffision weighted
Others: carotid imaging - doppler
Further management: anti-platelet (clopidogrel or aspirin & dipyridamole) and statin (atorvastatin 20-80mg daily)
Brain tumours
* Presentation
* O/E - fundoscopy signs for raised ICP
Progressive focal neurological symptoms, signs of raised ICP and systemic signs, altered mental state, focal seizures.
Papilloedema= swelling of the optic disc, elevtated optic disc, haemorrhages, Paton’s lines (folds in retina around optic disc), engorged retinal veins, loss of venous pulsation
Types of brain tumour
1.Gliomas (arise from glial cells in brain/SC) - 3 main types from benign to most malignant:
2. Meningiomas (arise from meningeal cells): effect?
3. Pituitary adenomas(arise from pituitary gland) can be secretory/non-sec. Sx due to hormone excess? (Or depletion):
4. Vestibular schwannoma/acoustic neuroma: Nerve origin, location, association
Gliomas:
1. Ependymoma
2. Oligodendroglioma
3. Astrocytoma - most common/aggressive is glioblastoma
Meningiomas:
- Generally benign
- Mass effect rather than invasive
Pituitary adenoma
1. Cushings (excess cortisol)
2. Acromegaly (excess GH)
3. Hyperprolactinaemia (excess prolactin)
4. Thyrotoxicosis (excess TSH, thyroid)
Vestibular schwannoma
- CN 8 (vestibulocochlear)
- cerebellopontine angle
- unilateral s/n hearing loss, tinnitus, dizziness +/- facial nerve palsy (compression on CN7)
Stroke mx
- Initial
- Intervention
- 2ndary prevention
Stroke & AF mx
-secondary preventiON
- how soon after stroke should this be started
Initial Aspirin 300mg stat (continue 2 weeks)
Intervention - thrombolysis - alteplase if within 4.5 hours of onset, thrombectomy - if last well between 6-24hrs ago, or if past 24 hours - bot (and if PCA/basilar artery or potential to salvage brain tissue)
2ndary prevention: antiplatelets; lifelong
1. Aspirin & dypridamole
2. Clopidogrel 75mg
+ Statin (atorvastatin after 48hrs)
If stroke + AF –> secondary prevention with anticoagulants, e.g. DOAC or Warfarin: apxaban AFTER 2 WEEKS
Malignant spinal cord compression
- oncology emergency
- extradural compression from tumour on spinal cord (lung, breast and prostate most common)
- features
- urgent investigation within 24hrs
- management
- urgent oncology assessment for consideration of:
- Back pain
- Neurological signs - increased reflexes below lesion, reduced at level of lesion.
- Paraesthesia and lower limb weakness
- Urgent MRI Spine
- High-dose Dexamethasone oral
- Consideration for radiotherapy or surgery
